December 31, 2009

Those of you who follow my postings know that I avoid most foods marketed as "low carb" and "sugar free" foods because they are so deceptively marketed. You have only to look at the latest fad food, Agave Nectar, to see the extent to which food companies will pervert science to make a buck.

Agave Nectar is sold as being good for diabetics because it doesn't raise blood sugar. What they don't tell you is that it doesn't raise blood sugar because it is full of fructose which goes directly to the liver after you eat it and turns into the intracellular liver fat that turns out to be a major cause of insulin resistance.

But I'm writing now to report on a low carb food that turns out to live up to the claims made for it, one that may be very helpful to many of us who are trying to keep carbs low.

I had been aware of these for years, as they are cited in many low carb recipes, but I avoided them as they used to contain soy protein and I don't eat soy protein because it has the ability to damage the lining of the gut allowing proteins into the blood stream where they provoke antibody formation and autoimmune attack.

But it turns out that Tova, the manufacturer has removed the soy protein from these products, and the only soy in them is a small amount of soy fiber, which I can handle.

I've been using these products for a month and am happy to report that they work as advertised. They have about 6 grams of carb per cup after deducting fiber and I have found no reason NOT to deduct the fiber as my blood sugar responds to these flours as if they did have 2 g per 1/3 cup serving.

The Carbquik makes a great Belgian waffle. It was nice to get out my dusty waffle maker and rediscover a great breakfast. Here's the "quick and dirty" recipe I use for 1 serving:

Stir up ingredients in order listed and pour onto your waffle iron. I top it with Vermont brand sugar free syrup (about 2 g of sorbitol) and defrosted frozen berries.

When it was time to do my holiday baking, I made two loaves of pumpkin bread, one with regular flour and one with Carbalose flour. The recipes were identical, which meant that I used regular sugar. This is because I wanted to know what changes the flour made that were independent of replacing the sugar with artificial sweetener. I doubled the baking soda as instructed by the Carbalose label.

The result was a loaf that was denser and moister than the flour version but most definitely a bread and quite delicious. The Carbalose loaf was also sweeter than it needed to be, which suggested that I could probably have made it with a lot less sugar. This was a lower carb food you could serve to people who loathe "diet" foods without hearing a word of complaint.

Even with the sugar left in, cutting out the flour made the pumpkin bread a lot kinder to my blood sugar than the unmodified version which is so full of carbs that even with insulin it tends to make me feel groggy.

Now that I know that the Carbalose flour replaces regular flour well, I will try it in some other baked goods and see what happens when I combine it with artificial sweeteners. I would not use it for a recipe that needs to be light and fluffy but it works well for moister things.

I also made biscuits using just Carbquik and water. They were a bit denser than regular biscuits but quite edible.

The product looks expensive, but you are buying Industrial-sized boxes and bags that should last you awhile. The 3 lb Carbquik box is surprisingly large and I still have about half of it left after making at least 20 single serving recipes.

I bought mine from Netrition because they host the very useful Low Carb Friends forum filled with helpful people who know a great deal about how to cut carbs and eat enjoyably. Their shipping is a flat rate of $5 no matter what you buy, so it is worth including some of the many flavors of DaVinci Sugar Free Syrup they carry in your order if that is something you use.

As far as how suitable these products might be for people dieting for weight loss, I am happy to report that I have actually lost a pound or so since I started eating the Carbquik waffles for breakfast. The high fiber content leads to a feeling of fullness. It's worth noting that as is the case with all high fiber foods too much can lead to gas, so I limit myself to one serving a day, which works well for me. Two was too much. But I did not experience any hunger or cravings after adding these products to my diet.

These products do contain gluten, so if you are gluten intolerant, they aren't for you. I am not wheat-phobic as are some people in the online health research community, as I believe it is the carbs in flour that cause the health problems attributed to wheat not anything specific to wheat except in the case of people autoimmune disease who are likely to have true gluten intolerance. But gluten should not be an issue for people who avoid soy and who do not have the inherited genetic profile that leads to gluten intolerance.

December 18, 2009

I'm taking a few weeks off from blogging to complete the revisions my editor at Avon requested to my upcoming novel, Lord Lightning. This is exciting work. Publication, though still many months away, is starting to feel a lot more real. But it takes a lot of concentrated mental effort to make the last small but important changes that make this novel irresistible, which is making it impossible for me to give my blog posts the kind of attention they deserve.

Next week none of us will be thinking of diabetes or--in many cases, diet. So let's plan to meet again in early January when many of us will be embarking on our annual repentance diet and others, it is to be hoped, will be resolving to get better control of their blood sugar.

Until then, I wish you, your families and your communities the very best for the holiday season and beyond!

December 9, 2009

I wrote a couple posts last year suggesting some diabetes-specific gift ideas and several of you wrote me that you found them helpful so I'm going to reprise the earlier suggestions and add a few more.

In the spirit of transparent disclosure, let me mention that some of these suggestions link to Amazon pages and if you visit Amazon using these links and buy things Amazon gives me 2-3% of the sale amount.

1. A Food Scale. I wrote a whole post about the power of the food scale to get your diet working again and fine tune insulin doses. You can read the whole post HERE

2. Pedometer, blood pressure meter, blood testing strips, etc. You can read more about all these gifts in this post HERE

3. Low Carb Treats. As most of you know, most of the products marketed as being "low carb" aren't, because they contain maltitol, lacitol, and other frankenfood ingredients which will, in fact, raise the blood sugar of anyone who does not have a very strong second phase insulin response. For this reason NEVER give a product labeled "sugar free" to someone with diabetes. They raise blood sugar and taste foul.

Fortunately, there are a couple low carb products that are truly low carb.

Here are some ideas:

a. DaVinci Sugar Free Syrups. These come in a multitude of flavors. They are sweetened with Splenda but have no additional sugars added the way that powdered forms of Splenda do. I use them as the sweetener when baking low carb treats like macaroons. I also use them when making low carb cocoa. One Tbs of syrup is the same as one Tbs of sugar when baking though you might bake recipes a bit longer to boil off the fluid. My favorite flavors are White Chocolate, German Chocolate, Caramel and Vanilla. One bottle lasts me a very long time and never goes bad.

b. Not Starch. This is a mixture of fibers that will thicken gravy or homemade ice cream very nicely. It gives a slippery mouth feel you will immediately recognize as it is used in so many frozen food and restaurant gravies.

c. Protein Powder. Look for one that has no more than 2 g of carbohydrate per serving. You can use these in shakes or you can bake a bewildering selection of low carb baked goods with these. Most include artificial sweeteners or stevia. I just bought a "Natural flavor" one that has no sweetener or flavor at all, which tastes just so-so but would be good for people who have concerns (whether or not justified) about artificial sweeteners.

d. High Quality Dark Chocolate. The higher the percentage of chocolate in a chocolate bar, the kinder it will be to your blood sugar. You can find many 70% and higher bars on the market today and if a person does not have problems with portion control they can make a very nice gift. Read the label and stick with chocolates that have no more than 6 grams per square if possible.

e. Gourmet Cheese. People have different tastes in cheese and some gourmet cheese has become very expensive in the U.S. because of our falling dollar, so find out what kind of cheese your favorite person with diabetes likes before investing. But if you know, you can't go wrong in buying them a premium cheese. I don't mail order these, however as I have yet to find a mail order company whose cheeses weren't filled with additives.

f. Steak. Low carb and delicious and available from mail order companies. Don't send mail order ribs or pork as they tend to arrive bathed in extremely sugary sauces.

g. Fancy Nut Assortments. Full of good fats and delicious. Don't give these to someone who is actively pursuing weight loss, though, as most of us have trouble eating "just one."

h. Gourmet Coffee. The very best coffee I have ever tasted is available by mail order from Dean's Beans. Dean is a real person who I've met. He is obsessive both about buying beans in ways that benefit the people who grow them and the enviornment and finding the most delicious beans available. My personal favorite is the "Half caf" blend which is 1/2 strength but richly flavored. I also like the "Rattlesnake Gutter" blend, named after a local ravine, and the "Liberation Decaf." Dean's baking cocoa makes extremely delicious cocoa when mixed with DaVinci syrup, half and half and boiling water.

i. Fancy Tea. You can find wonderful tea at http://cookscorner.net. Some of the fruit blends contain pieces of real fruit mixed with hibiscus, calendula, rose hips, and other herbs. They are delicious and I have not found that they raise my blood sugar. The Apricot and blood orange pear are my favorites. If you are on a budget, you can find many delicious teas in any large supermarket or health food store.

Please post your own gift suggestions for people with a diabetes in the comments!

December 7, 2009

A study described in last week's Science Daily points to a problem that has been troubling me about diabetes research: the way that research relies on rodent models that are built on false assumptions about the human diseases they are supposed to model.

You can read about the study describing severe problems with the mouse model for Muscular Dystrophy here:

... two major features of a key DMD [Duchenne muscular dystrophy] gene are present in most mammals, including humans, but are specifically absent in mice and rats, calling into question the use of the mouse as the principal model animal for studying DMD.

This is bad news for people who have been waiting for scientists to find treatments for DMD but this kind of problem is not limited to research on DMD.

A huge amount of "diabetes" research is conducted in db/db mice, ob/ob mice, the New Zealand Obese (NZO) mouse, and Goto-Kakisaki Wistar Rats. A small group of highly respected scientists have built their careers around their knowledge of these particular mice and rats and sent their students out into the academic world where they have spread the use of these rodent models.

The problem is that these rodents became models for human Type 2 diabetes because of their phenotype--i.e. symptoms--matched what researchers 25 years ago thought was the phenotype of Type 2 human diabetes.

They are very fat. They become fat eating high fat diets. The blood sugar of these rodents worsens when they eat fat. Low carb diets are very damaging to these rodent models. In short what we have here is a model of outdated assumptions about Type 2 Diabetes that have not been proven true in humans with the disorder.

Humans with Type 2 diabetes may be fat or of normal weight. Most become fat eating high carbohydrate diets. Human blood sugars usually improve when they eat low carb diets.

The reason that the rodent model does such a poor job matching human experience becomes clear when we look at the genotype of these rodent diabetes models. Their broken genes are not the broken genes found in humans with Type 2 Diabetes.

The ob/ob mouse, for example, is morbidly obese as are many humans with Type 2 diabetes. However, the ob/ob mouse is obese because it has a genetic flaw that keeps it from producing leptin. This makes this mouse catastrophically hungry. But it turns out that after 6 years of hunting for leptin deficient humans, researchers found a grand total of three human familiesin the entire world who have the same genetic flaw as the ob mouse. Everyone else on earth who is very fat has some other genetic issue causing their morbid obesity.

You would think this discovery would have put an end to the use of the ob/ob mouse in diabetes related research, but you would be wrong. The scientists who have built their careers on their expertise in using this one mouse don't give up easily.

A Google Scholar search for studies conducted after 2005 where ob/ob mice are used as a model for diabetes turns up hundreds of studies.

The db/db mouse is another popular mouse model for diabetes. It is described thus:

"Diabetes (db) is an autosomal recessive mutation located in the midportion of mouse chromosome 4 that results in profound obesity with hyperphagia [compulsive overeating], increased metabolic efficiency, and insulin resistance.

The only problem with this model is that the genes that make the db/db mouse seem to resemble a diabetic human are NOT the genes that have been found in diabetic humans.

This is the problem with all the rodent models of Type 2 diabetes. No one questions that these rodents might have insulin resistance or that they might overeat. But over the past decade the dramatic drop in price of genetic screening techniques has come up with a long list of the most common genes associated with human diabetes. In European populations the list includes genes like TCF7L2, HNF4-a, PTPN, SHIP2, ENPP1, PPARG, FTO, KCNJ11, NOTCh3, WFS1, CDKAL1, IGF2BP2, SLC30A8, JAZF1, and HHEX. Failure of any of these genes can produce diabetes, but the exact phenotype of that diabetes will vary because what is broken is different.

People from non-European ethnic groups have been found to have entirely different sets of diabetic genes, like the UCP2 polymorphism found in Pima Indians and the three Calpain-10 gene polymorphisms found associated with diabetes in Mexicans. As a result the "natural history" of their "Type 2" diabetes is quite different than that of Europeans and they develop different patterns of complications than do people of European backgrounds.

"Diabetic" mice and rats do not have any of these human genetic flaws but other, rodenty gene flaws that give them rodent "diabetes." This does not mean it isn't useful to explore their physiologies, only that we must always keep in mind that they are different from those of humans diagnosed with Type 2 Diabetes--just as individuals diagnosed with "Type 2 Diabetes" can differ dramatically from each other.

The chances that any finding in mice might cross over and apply to humans is very slim. When these studies are reported to the media they should not be reported, as they are now, as if they applied to humans.

Beyond this issue, though, lies the problem pinpointed by the Muscular Dystrophy researchers. The mouse is very different from the human being, physiologically and genetically, in ways that researchers have not probed because, face it, the people who know the most about how to study mice are precisely those whose careers come to a crashing end if mouse research ever goes out of fashion.

We don't know enough, yet, about the genetic differences between rodents and people to know how the genes expressed in the livers of mice differ from those expressed in humans. Until we do, it is pointless to study what pattern of macronutrient intake causes fatty liver in mice. We don't know enough about the many genes involved in the regulation of glucose in the pancreas or brains of mice either. The Muscular Dystrophy research discovered that the genes expressed in the brains of people were significantly different from those of mice.

Glucose regulation in any species involves a complex symphony of interacting feedback loops involving gene expression in the brain, liver, pancreas, muscle and gut. The chances are very high that, because of significant differences between human organs and rodent organs, the findings drawn from rodent research--which form a much more significant part of "what everyone knows about diabetes" in the medical world have led us into dangerously wrong blind alleys.

The value of the low fat/high carb diet for people with diabetes was supported by immense amounts of rodent research. Unfortunately, what that research proved was that fat is a problem for rodents whose diabetes is caused by mutations unrelated to those found in humans which disorder metabolic processes quite different from those that occur in humans.

It is possible that there are proteins in humans that are significantly involved in the production of human forms of Type 2 diabetes that mice don't have or that they don't use the way humans use them. By concentrating so heavily on rodent research, researchers may be missing these vital proteins and the impact of the genes that code for them.

But mice are cheap, live brief lifespans, and can be "sacrificed" without causing massive protests. The students of the original mouse expert researchers have grown into a huge grant-gobbling research establishment that thrives on doing mouse research. It isn't going to go away soon.

Another study published just last week shows that another entrenched group is hoping to get their share of the lucrative diabetes research dollar. Lo and behold, they've created a Fruit Fly Model of Type 1 Diabetes. You can read about it here:

"These mutant flies show symptoms that look very similar to human diabetes," explains Dr. Pick. "They have the hallmark characteristic which is elevated blood sugar levels. They are also lethargic and appear to be breaking down their fat tissue to get energy, even while they are eating -- a situation in which normal animals would be storing fat, not breaking it down."

I have friends who are highly distinguished fruit fly gene researchers and I have immense respect for the work they do, but they are doing basic science looking, for example, at the genes that produce neurons to better understand what a neuron really is.

I am left scratching my head to understand how a fly that lacks blood vessels, a liver, or pancreas can be a "model" for human autoimmune diabetes. A fly with high blood sugar is not a fly with "Type 1 Diabetes." And by the same token, a fat fly that eats too much may be an interesting fly that may teach us something new about fly physiology, but it is not a "Type 2 diabetic" fly.

Diabetes is a set of symptoms produced as the end result of failures at various points in a complex organism with its own evolutionary history. It is not a single condition. It is not caused by a single failure of one gene that can be explored at the level of basic science.

Until doctors and the public understand this better, we will continue to be subjected to "medical truths" derived entirely from the same kind of rodent research that has already set back the treatment of the vague collection of symptoms called "Type 2 Diabetes" for decades.

December 3, 2009

Interlibrary loan sent me a copy of the book, Mummies, Diseases and Ancient Cultures recommended by a knowledgeable blog commentator, but unfortunately it turned out to be the first edition published in 1980 not the updated one from 1998. I'm using an extended ILL feature to request the newer version, but meanwhile I read through the first edition and found it fascinating.

Relevant to the topic of my blog here was one theme that stood out in analysis of all the ancient bodies that had been preserved through time: Ancient people, no matter what time period they lived in or where they lived, carried a significant load of parasites.

The parasites most commonly found in these munmies included hookworms, tape worms and the roundworms that cause trichanosis. Besides sickening us, these parasites can make a significant difference in how we metabolize foods.

The tapeworm, for example, allows people infected with it to live out the dubious fantasy of "eat all you want and never gain weight." Unfortunately, when this happens in a situation where the food supply is marginal--i.e. just about everywhere on earth before the 20th century--worm infestation can predispose people to starve to death.

The roundworms lay eggs in human muscle, which probably produces inflammation, though they also can infect nerves and the brain. In either case, they have a strong effect on metabolism.

Parasites get into our bodies in many ways. Some come from eating meat that hasn't been thoroughly cooked. Some are carried in water where other animals have defecated. Some enter the body from the soil. Others are transmitted by insect bites.

Because parasites were such a common feature of life until very recently, it makes sense that our bodies are highly adapted to live with them. And because the loss of the usual human parasites load is so very recent, some scientists who study the development of the human immune system speculate that the current explosion of autoimmune disease is partly caused by changes in the way that the immune system develops in children whose immune cells don't encounter parasites early in life.

However, while there may be something to this theory, there are plenty of other factors besides parasite exposure that also explain the increase in autoimmune diseases. And a big problem with the parasite explanation is that it doesn't explain why this explosion in diagnoses only kicked in about twenty years ago.

My belief is that the invasion of our food supply by soy protein and its ability to damage the gut and make it permeable to proteins like gluten is probably a better explanation for the changes seen in the past generation. I've discussed that theory HERE.

Still, there is no question that the elimination of parasites from our system is a huge change in human health and one that only took place in developed nations during the past century.

Caleb Finch, a gerontologist from the University of Southern California (USC), has come up with an intriguing theory, published in December issue of Proceedings of the National Academy of Sciences that links the loss of our parasite burden with the increase in heart disease and Alzheimers.

His theory explains the fact that humans have much longer natural lifespans than apes, as a result of their having developed new gene variants that allow them to tolerate the higher burden of inflammation that comes with eating a meat-rich diet.

You can read the text of the press release describing this study sent out by USC displayed here:

"Over time, ingestion of red meat, particularly raw meat infected with parasites in the era before cooking, stimulates chronic inflammation that leads to some of the common diseases of aging,"

From reading the Mummies book, I would correct this statement, because the data reported in the mummies book makes it very clear that ancient meat-eating humans who did cook their food still carried a high load of meat-borne intestinal and muscle parasites.

But Finch goes on to explain that one way humans adapted genetically that allowed them to flourish with a higher burden of meat-borne parasites is by evolving a human-unique form of Apo(E).

Finch is quoted as saying,

In addition to differences in diets between species of primates, humans evolved unique variants in a cholesterol transporting gene, apolipoprotein E, which also regulates inflammation and many aspects of aging in the brain and arteries.

Other primates who do not have the human forms of Apo(E)develop heart disease very quickly if they eat diets rich in meat, an argument that is often cited by those promoting vegetarian diets.

Still, unlike gorillas who develop heart disease in just a few years after adopting a meat rich diet, humans eating meat-rich diets do not develop heart disease until they are in middle age-- after they have reproduced, which Finch links to the human-only Apo(E) variant. And later-onset heart disease because it happens after reproduction does not impact evolution.

Finch does not pursue this point, but it strikes me that this argument suggests that the loss of the usual human parasite load may also partially explain why the incidence of heart disease has increased over the past century--the period in which humans for the first time cleaned up water supplies and eliminated wild meats with their high parasite load from their diets.

It is possible that when the immune system is not kept busy dealing with a high level of inflammation caused by invading parasites it is more apt to attack cardiac tissue. Recent research suggests very strongly that heart disease is an inflammatory condition. There are also intriguing hints that morbid obesity may be linked to inflamed fat tissue.

None of these theories are fully fleshed out. Though Finch's finding that only humans have the special forms of Apo(E) required for primates to metabolize meats should give us another reason to ignore ALL diet research performed in rodents or other non-human species because these other species do not carry the human adaptations to meat eating that Finch suggests are a large part of why humans have evolved so successfully.

Beyond the changes that allow us to eat parasite-infested meat safely, there are probably human physiological adaptations to parasites that impact on our ability to store fat in an environment were we are competing with parasites for the nutrients in our food.

This suggests to me that followers of the so-called Paleo diet cannot faithfully reproduce the supposed health effects of that diet unless they have taken on the load of intestinal worms early in life and allowed them to mold their immune systems and other physiological parameters.

Even adding these worms in mid-life won't help because, as Sachs' book explains, the balance of the kinds of T cells produced by the immune system throughout life seems to be shaped by the antibodies transmitted from the mother (infected with parasites in a true Paleo state) and the organisms the young creature encounters early in life.

Without a gut full of worms no one is eating a true Paleo Diet. Which is another reason to avoid extremism in dietary theory and to eat a diet that resembles that which your long lived ancestors in the past 150 years were eating.

The Colonial era graveyards in rural New England where I live are filled with graves of people who lived into their late 80s and 90s. Those who died young typically died of infectious disease, child birth, or, surprisingly frequently, fire and drowning.

We know a great deal about their diet. It was made up of fresh meat in summer and fall, salty preserved ham, salt beef, and lots of salt cod the rest of the year, dried fruit, corn meal, wheat, squash, turnips, and potatoes, preserves made with sugar, and milk, butter and cheese.

Nanoparticles are extremely tiny particles, which are found rarely in nature--for example in metallic ceramic glazes--but they only came into prominence over the past 15 years when modern manufacturing technologies made it possible to make them in bulk. They are used for hundreds of applications, from enhancing the sparkliness of cosmetics, to making fabrics stain resistant, and to delivering drugs.

These particles are so tiny they can easily move through cell membranes in ways that normal sized particles cannot. But because many of these new nanoparticles are made out of commonly occurring minerals considered safe--like the titanium dioxide which was the subject of the above study--they moved out of the lab into consumer products without the kind of extensive safety review they should have been given.

The study above found that when mice drank water with titanium dioxide nanoparticles in it, the particles concentrated in their organs. Their bodies have no way to eliminate them since these kinds of particles are very rare in nature.

Worse, because these nanoparticles are so tiny they can pass through cell membranes, the research cited above found they caused "genetic instability" and DNA deletions. They also caused inflammation.

There are many rodent studies that must be viewed sceptically, but that research is inevitably research involving high level functions like the balance of macronutrients in an animal's diet. But this research looks like it would apply to any mammalian cell. And that means these same water-borne particles that get into the mouse organ also pass through human cell membranes with devastating effect.

If if that is the case, we are all in huge trouble, because these nanoparticles are everywhere. Here's what the chief researcher on the above study explained:

The manufacture of TiO2 nanoparticles is a huge industry...with production at about two million tons per year. In addition to paint, cosmetics, sunscreen and vitamins, the nanoparticles can be found in toothpaste, food colorants, nutritional supplements and hundreds of other personal care products. [emphasis mine]

.An study published this past March found that these particles are being discharged into waste water and making their way into the environment in amounts that have the potential to damage life forms at all levels.

Referring to the nanoparticles found in cosmetics, the chief researcher in the March study explained,

... the particles are washed down the drain in homes as people bathe and end up in municipal sewage treatment plants. From there, they can enter lakes, rivers, and other water sources where microorganisms serve essential roles in maintaining a healthy environment.

She also studied survival of Escherichia coli (E. coli) bacteria when exposed in laboratory cultures to various amounts of nano-TiO2.

She found surprisingly large reductions in survival in samples exposed to small concentrations of the nanoparticles for less than an hour.

Another study reported in this same article found that another microorganism

... cannot tolerate silver, copper oxide and zinc oxide nanoparticles. Toxicity occurred at levels as low as micrograms per liter. That's equivalent to two or three drops of water in an Olympic-sized swimming pool.

You Have No Way of Knowing What Products Contain Nanoparticles

Because labels only indicate the chemical name of an inorganic substance, not the form in which it occurs in a product, you have no way of knowing if the drugs, cosmetics, or supplements you use contain these particles.

Nor is titanium dioxide the only nanopartcles that is being used in industrial quantities. Nanoparticle versions of silicates and other metal oxides are everywhere. Silver nanoparticles are used in antibacterial applications. Nanoparticles are used in clothing to make socks resistant to odor. Wash the socks and particles enter the water supply. They are in sunscreens. They are in stain resistant fabrics.

The nanoparticle business is huge and the companies profiting from selling these "high tech" substances are not going to give them up without a fight. Only the big chemical companies and their customers know what other nanoparticles might be in products you buy. Clothing, carpet, and furniture are likely candidates, given the increasing use of nanoparticles in fabric.

Nanoparticles in fabrics and cosmetics supposedly do not go through the skin, but that should not make you feel safe because of the way they eventually reach groundwater when you bathe. And because they are also being added to pills and perhaps foods none of us can feel safe.

A quick scan of my calcium supplements shows that they contain silicon dioxide--low on the list of ingredients, which suggests that it occurs in a small quantity. Silicon dioxide is more familiar to us under its common name, "Sand." Given the lack of grittiness in my calcium pill it's likely that this is a nanoparticle introduced to make the supplement look better.

I can't tell you what is in my metformin because there is no requirement that the drug company furnish me with a list of ingredients. However, it is very possible it too contains a nanoparticle introduced to make its whiteness look "purer."

The history of asbestos gives us a good idea of how long it takes to get a dangerous substance out of our environment--decades after lab research has clearly defined its toxicity. Asbestos was mostly used applications where it could be easily identified, not in food, clothing, drugs, and cosmetics.

Given the weakness of our regulatory bodies and the strength of the chemical industry, chances are that what we have here may be an ecological and medical catastrophe that may dwarf anything we have hitherto seen. It will take a decade or two for the effects of nanoparticles to become so obvious even the chemical industry must admit they are real. Because they are so universally distributed, it may be very difficult to link them to the effects they create.

With every new piece of research pointing to the dangers, the chemistry industry will respond, "More research needs to be done" the way they did with asbestos and the way that the cigarette companies did with tobacco.

By the time the danger is understood, these particles will have dispersed through our environment and our bodies in ways that may be irreversible.

November 18, 2009

No, this is not a post about the "eating fat causes heart disease" fantasy, nor is it a post about Going Rogue, but the issue I am going to discuss here shares features with those topics the Low Carb community has been very resistant to confronting.

The issue is this: The very same people who spend hours hunting through overlooked but well-designed published medical research to provide us gems that help us understand metabolism better seem to lose their respect for scientific method as soon as they turn their attention to theories about human prehistory.

People I otherwise respect greatly accept theories about "paleo diets" and the health of early human populations that are either a) based on a very small sample of outdated early 20th century research or b) entirely made up.

It may come as a surprise to some of you that the study of paleontology is a scientific discipline pursued by intelligent, educated scientists using a wide variety of sophisticated tools. These scientists have come up with many findings that tell us a lot about the lifestyles of real "paleo" peoples around the globe.

None of this research is ever cited by the people who have made the so-called "paleo diet" a religious crusade, people who have never taken the time to look into the evidence these myths are based on.

Paleo Fanatics Show Off Their Ignorance

Just this week I read a post on a Low Carb discussion board claiming that the Egyptian mummy that shows evidence of heart disease came from a period "right after the invention of agriculture"--a statement which in off only by about 11,000 years. Agriculture started somewhere around 12,000 BC and the earliest of these mummies are from about 1600 BC.

By the same token, we know a great deal about the lifestyles of hundreds of modern day hunter gatherers painstakingly collected by trained anthropologists who lived with these people for many years. You would never know this from reading the Paleo fantasist's writings, which invariably cite one and only one source, the early 20th century arctic explorer, Vilhjalmur Stefansson.

A recent correspondent went to far as to inform me, based on what he had read on a Paleo fanatic web site, that Stefansson was the only person to ever live with a hunter gatherer culture while speaking their language. This misstatement ignores the work of at least 400 other trained anthropologists who not only did the exact same thing as Stefansson, living with people of pre-industrial cultures all around the world, but in many cases they lived with these people for far longer than the few winter months Stefansson did. They also published more extensively about their observations in writings intended for other anthropologists, not a popular audience, and those writing later in the century were much more aware of the need to see ALL of what was going on in the culture, rather than cherry pick the cultural details that reinforced their personal beliefs and ignore the rest.

So with this in mind, you can see why I find it disturbing that people with a lot of cred in the Low Carb world, including several of the M.D. mega-bestselling authors, continue to parrot Paleo fantasy statements about "our ancestors' diet" or about the diet and lifestyle of modern non-agricultural peoples that have no more basis in science than the idea that eating fat gives people heart attacks.

What Science Knows About Real Paleo Diet and Lifestyle

If you are interested in learning more about what our ancestors really ate, I would highly recommend a new book written by a brilliant Harvard anthropology professor. It opened my eyes to the advances that have occurred in paleontology since I studied it at the University of Chicago in the 1960s when I took my Anthropology degree there.

Wrangham's book's very-well documented thesis is that it was the very early discovery of cooking by pre-human hominids which allowed humans to develop the metabolically expensive human brain. His main point is that cooking, because it breaks down starches and proteins, made redundant the long, metabolically expensive digestive tracts found among pre-human hominids and allowed them to atrophy, freeing up the calories no longer needed for 5 hours a day of chewing and round the clock digesting of raw foods to be used to fuel, and grow, our metabolically expensive brains.

But the relevance of this book to our discussions in the online diet community lies not so much in its primary thesis but in the mass of data, derived from extensive research, the author provides about what the historical and anthropological record tells us about what early humans and prehumans ate.

And that research makes it clear that people and "pre-people" eating pre-agricultural diets bear little relationship to the Supermen described in the Paleo Myth invented people ignorant of paleontology and anthropology.

For starters, in most of the many modern era hunter-gatherer societies studied since the late 19th century, it turns out that at least 50% of calories came from gathered, i.e. vegetable, sources not meat, almost always provided by females. And even more importantly, these gathered foods were not made up of leaves which provide very little nutrition, but of starchy foods especially roots, seeds, and tubers.

Wrangham also cites the finding that the Inuit, so beloved by Paleo fantasists, ate more than fat and meat: they savored the raw, full intestines of their prey as well as deer droppings. This suggests the lengths to which humans will go to get the nutrients found from plant-derived sources--and how inadvisable it is to use the Inuit as the model upon which to base your diet.

Nor does research substantiate the idea that the lives of ancient Paleo people were the easy, physically invigorating idylls the Paleo myth describes. Hunting in most environments is an exhausting pursuit that provides marginal sustenance. The usual prey is not an elephant but a few small rodents. In most modern era pre-agricultural societies the sheer volume of food-related labor women are forced to provide is comparable with what was demanded of plantation slaves or the most oppressed factory worker.

The fantasy is that Paleo people lived lives of unparalleled health until they were forced into agriculture and made to live on evil carbs. The reality is that the bones of our "paleo" ancestors show clear signs that they were subject to periodic, severe and crippling famines.

This finding is, of course, reinforced by reports from those who had first contact with modern era hunter gatherers. It is often forgotten that one of the reasons that the earliest French settlers of Canada had so much contact with Native American tribes is that the tribes were starving when Champlain first encountered them, and they came to the French because they offered food.

Wrangham also points out that in modern Africa traditional people's must contend with a long period during the Dry Season when famine is common when game disappears.

I recently read a fascinating biography of a 19th century white child who was raised by Californian Native Americans living a traditional lifestyle, The Blue Tattoo: The Life of Olive Oatman (Women in the West) which made clear what it would be like to live through such a periodic famine. It describes one that occurred in a traditional non-contact Native American society living in SE California. Summary: many children died as did many older adults.

People adopted agriculture because it gave them a much better chance of seeing their children survive. Women probably put a lot of pressure on their men to adopt the agricultural lifestyle because as hard as women work in agricultural societies, their lot in them is far better than those of women in pre-agricultural societies who may have to gather and drag 30 lbs of roots over a range of ten or more miles every single day--before they start cooking dinner for men just returned from hunting.

It is worth remembering that those very few pre-agricultural societies that survived the agricultural revolution--the ones observed by Stefansson and others--were all cultures where people lived in environments where hunting and gathering provided more food than agriculture could--areas with very short (or in the arctic, no) growing seasons, deserts, areas with disease vectors that made settled life fatal, or very rarely, as in Amazonia and New Guinea, tropical areas where nature provided much more food than it does in the temperate zones.

Everywhere else, hunting and gathering was a very hard way to stay alive, and people took to agriculture with the alacrity with which our generation has taken to the computer and for the same reason: because the benefits were undeniable and instantly obvious.

Grain-based agriculture let more children survive to adulthood. Only after its advent did the human population begin to grow at a steady rate, rather than just barely replacing itself.

Grain-based agriculture provides, uniquely in human experience, enough surplus food that some people can put their time into non-calorie producing behaviors, like inventing writing which allows shared knowledge and technology to grow beyond what one person can retain in their memory. It is those grain-provided surplusses that have led to your being able to sit in front of your computer reading this post even if you do it while imagining how much happier you would be if you were "Paleo Man."

Why Does It Matter?

Okay, you might say, maybe the whole Paleo thing is a myth, but why make a big deal about it?

The answer is simple. The minute you support a good idea with made up "facts" and bad science, you invalidate it.

Doctors and nutritionists ignored the Atkins diet because he supported his claims with outdated, discredited studies like the one describing "fat mobilizing substance" and the research that claimed someone lost a huge amount of weight eating ten thousand calories a day of fat. By relying on bad science (and not updating the books to remove it, long after it was known to be bad science) Atkins delayed for a generation the rigorous study of the low carb diet.

We run the risk of doing the same thing to the diet when we argue for it using myths that educated people know to be myths.

What makes it so sad is that there is no need to use myths to make our point. There is plenty of very good science that supports the advantage of cutting down on carbs, eliminating processed foods, and demanding that industry stop polluting our environment with organic chemicals that are damaging our bodies We don't need to argue for our modern dietary improvements by citing imaginary, Eden-dwelling ancestors and misrepresenting their diets to do it.

The truth is, it is irrelevant what ancient people ate 20,000 years ago. Evolution occurs in periods as short as 100 years, so the dietary changes that have taken place in that past 20,000 years have altered our metabolic physiology in thousands of small ways that make us very different physiologically from "paleo" people.

To see an example of this, we need only remember that those of us who are descended from herders can digest milk as adults, while those who did not evolve in cultures with domesticated milk-giving animals are lactose intolerant, like most other adult mammals.

So matter what Paleo peoples ate, those of us who descend from European or Asian stock living in the Temperate Zone can be sure our ancestors' bodies adapted very well to agricultural diets. We are all descended from people who flourished on the energy provided by the stored starchy vegetables and grains that kept them alive through the long cold northern winters when game is very hard to find. Those who did not flourish on those diets did not survive to become anyone's ancestors.

It's Not The Deep Past But The Very Recent Past That Points to The Problems

Rather than imagining the far distant past, we need only look at the very recent past to find much more relevant arguments to support our need for dietary change.

It is the new factors introduced in the past century that we should be focussing the full force of Science on to answer the question of why we have a sudden epidemic of metabolic diseases. Research is turning up a lot of answers, though the corporate-owned media ignore those that point to corporate culpability as the explanation.

The obesity/diabetes epidemic is closely related to the phthalates and other organic molecules that leach from PVC plastics and Bisphenol-A that estrogenize our bodies, the soy proteins that damage our gut linings allowing otherwise benign gluten to get into our blood stream an provoke autoimmune attack, the high fructose corn syrup that turns into intracellular liver fat, the arsenic from coal burning that promotes diabetes, the PCB, pesticide, herbicide and pharmaceutical drugs that are in our water supply and our bodies which all increase insulin resistance.

Let's focus on the real science and make the public aware of the findings of this good science so we can do something about this metabolic epidemic. Until we can heal it, those of us who can't process carbs will have to cut way back on them. But let's leave the myths that reinforce personal belief systems to the churches where they belong. They won't cure what ails us.=====UPDATE: Nov 21, 2009:

Check out this fascinating look at Arctic mummies. The link was posted by "Coach Jeff" in the comment section. The book cited is a real eye opener. I will have go get a copy.

Two of the Arctic and Aleutian mummies described here--those of older people--show distinct signs of atherosclerosis. The starved child who died with a tummy full of gravel and hair points out the impact of cyclical starvation on hunter cultures.

November 16, 2009

As we head into the holiday season it's time to reflect on a food-related issue that doesn't get the respect it deserves: portion size.

A study discussed in Science Daily last spring comes up with a fascinating finding about how our minds work--one that explains why we may find ourselves stalled on diets or seeing inexplicable rises in blood sugar. When presented with pictures of the same food in two different portion sizes, people disregard the differences in portion size when estimate calories. Instead, they seem to take a "unit" approach. One plate of food equals one serving.

All diet strategies that rely on counting anything will fail if you are estimating counts based on a nutritional database but ignoring the fact that the counts apply to a specific portion size.

Because the portion sizes given in nutritional databases are often much smaller than the portions you are likely to find on your plate you may think you are eating a certain food plan while actually eating two or even three times as much food than you think you are.

This tends to be true of all of us, no matter how aware we may think we are about what we are eating. The best way to deal with it, if you are having trouble controlling either your blood sugar or your weight, is to get yourself a digital food scale and start checking the portion size of the portion you are eating against the portion size given in the reference you are using.

You may quickly find the explanation for why your blood sugar is spiking after eating a food that used to work for you or why you have stalled on your diet.

Portion Size Issues Occur With All Macronutrients

The impact of getting clear on actual portion size will be greatest with foods that contain significant amounts of carbohydrate, because these fluffy foods are often the hardest to estimate. The carb counts given in nutritional guides for breads and cakes, for example, universally use a portion size of about 1.5 ounces for a slice of bread and 2 ounces for a muffin, roll, or piece of cake.

Years ago it is possible that someone did sell 2 ounce muffins, but when I went out last year and started weighing baked goods friends brought over I found that the bakery cookies being sold in my town ranged up to 5 ounces each and the coffee shop muffins were often as much as 7 ounces each. Artisanal bread can easily clock in at 3 ounces a slice, too.

Many people with diabetes can tolerate a 10 g serving of carbs. Some, larger people can even tolerate 15 or 20 grams at once. So if you consult your nutritional guide and see that a single chocolate chip cookies is listed at 9 grams, you may easily end up eating "one" five ounce cookie (or even a "small" 2 ounce cookie) without realizing that the database-supplied carb count was based on the size of one boxed ounce chocolate chip cookie which weighs one half of an ounce--15 grams.

The same is true of pasta. Some people with diabetes can eat pasta, because it does digest very slowly and if they have a slow second phase insulin response, it may be enough to mop up the slowly released carbs. But this tends to be true only if you eat a 2 ounce portion of pasta--the portion listed on the box. The portions of pasta sold at restaurants are anywhere from 6 to 8 ounces of pasta. Far too much for anyone to handle, both in terms of carbs and calories--and we haven't even gotten into the issue of sauce. When was the last time you got 6 servings from one can of bottled spaghetti sauce?

But portion size is not only a problem when you eat carbs. When you eat a very low carb diet, excess protein gets converted into glucose by your liver. So if you are eating far more protein than your body needs to repair muscle or provide the small amount of glucose your brain requires, the rest of the protein you eat will turn into glucose in the liver through a process known as "gluconeogenesis."

This happens very slowly--over about 7 hours, but it can be one reason why people eating low carb diets develop rising fasting blood sugars. If you ate a huge protein portion for dinner, after eating a lot of protein at lunch, the cumulative impact of the glucose derived from that protein on your blood sugar may not show up until the middle of the night. Protein shakes pose the same kind of problem, which is why a diet that involves eating large protein shakes for breakfast and lunch may have a very bad impact on your blood sugar, no matter how "low carb" it purports to be.

Meat portions are very hard to estimate. When I started weighing food a few years ago I found I was almost always underestimating meat portions which could easily be twice as heavy as I thought they were. A 300 lb man might be able to lose weight eating a 12 ounce serving of meat at every meal. A 145 lb woman probably can't.

Fat portions matter too if you are trying to lose weight. When you are eating a very low carb diet it is often possible to eat a lot more fat than you could eat on a standard diet and still avoid weight gain. This is because the processes that lead to fat storage tend to be blocked or slowed down when you are in a ketogenic state.

But if you are trying to lose weight eating too much dietary fat will stop weight loss cold, because it is much easier, physiologically, for your body to burn dietary fat than it is to break down the fat stored in your adipose tissue. So if you are eating more fat than you need, you may see weight loss come to a stop. This is especially likely to happen once you have lost 10-20% of your starting weight--a point at which the body's hormone balance becomes one that is much more conservative about releasing stored fat.

The portion sizes of high fat foods are very hard to estimate because they are so dense. The difference between 1 ounce of cheese and 2 ounces is not a lot. Weigh out one portion of peanut butter as listed on the label you will find realize that most of us eat two "portions" any time we eat peanut butter, if not more, without realizing it.

Be Careful What You Put on Your Plate

The study I alluded to at the top of this post has something else to teach us. Because our brains tend to treat whatever is on our plate as "a portion" it's a very good strategy to make sure that you only put onto your plate exactly what you intended to eat. This really comes into play during the upcoming holiday season where food has a way of showing up on your plate almost as if by magic.

Don't kid yourself that you will only eat "a few bites" of a serving of food that ends up on your plate. You'll do much better if you only put on that plate what you intend to eat. If this turns out to be hard to do--and for many of us it is--if you want to eat "a few bites" of some nutritionally horrifying but emotionally satisfying holiday food, ask a close friend or spouse to take the food onto their plate and then only transfer to your plate the "few bites" portion it is safe for you to eat.

I have on occasion had my Sweetie put overly-appealing holiday food gifts into the family safe and had him dole them out to me on a preset schedule. This can make the difference between enjoying a daily 10 gram treat and experiencing a 100 gram metabolic melt-down.

Planning for the Holiday Food Orgy

When it comes to setting the boundaries, it's worth reminding yourself that no one ever gave themselves retinopathy or caused a 30 lb weight gain eating one special high carb high fat high calorie meal. What messes us up is eating that kind of meal over and over again.

Unfortunately, the holidays we celebrate them now, stretch out into a six week period in which "special" holiday meals can appear daily or even two or three times a day for weeks at a time. And this does pose a serious problem for those of us with damaged metabolisms.

Many of us find that the safest strategy is to plan ahead. We choose the specific days or meals where we will eat whatever we decide we are going to let ourselves eat. These are scheduled events, NOT meals we "schedule" on impulse when confronted with a table unexpectedly loaded with tempting delights.

We prepare for those days of holiday excess by eating very carefully for the weeks before they happen. And we know that we will have a tough day after that holiday feast is done--a day when you will be hungrier than usual and will have to exert some very strong will power to avoid making a "one time" indulgence a daily habit.

If you have run into problems in the past at holiday time, being realistic about what is likely to happen, and planning for controlled indulgence, may work out better for you than resolving on complete abstinence and having the unplanned indulgences overwhelm you.

But if you do end up eating more than you intended over the holidays, don't beat yourself up over it. Only people living in caves with no access to the media who have no friends or family--or whose entire circle of family and friends is made entirely of dedicated health nuts-- get through the holidays without a dietary struggle, and only people with very rigid personality struggles win that struggle easily.

I wrote it years ago for the general dieter, not necessarily someone with diabetes, but you will find that even if you do not produce insulin it may still be helpful. Since I wrote it I have learned more about the hormonal factors that influence hunger, and I now suspect that these other hunger-related hormones play as much of a role as insulin does in producing the rebound hunger you experience when you eat a lot of foods you've been avoiding on a diet.

But the physiological explanation for the phenomena that occur after you crash off a diet are not as important as is learning a strategy that will keep you from turning a one-time food fest into a month, or year-long binge. The strategies I've described in the web page work very well.

Read the article BEFORE you head out into Holiday Food World. This is definitely a situation where preparing yourself before you get into trouble can make it a lot easier to get out of trouble.

November 12, 2009

The latest study to compare low fat with low carb diets came up with the finding that long term the Atkins diet caused more mood problems than the low fat diet. This has caused a flurry of posts from LC bloggers and forum participants dissing the study. But I've had a good look at it and I think people are missing some very important things when they dismiss this study outright.

The most significant finding of this study, which seems to have escaped everyone who has written about it, is that it contradicted the earlier, and very heavily publicized, finding that the low carb diet caused problems with memory and thinking.

This year-long study found Working memory improved by 1 year (P < .001 for time), but speed of processing remained largely unchanged, with no effect of diet composition on either cognitive domain.

So that should put to rest any concerns you might have had about the impact of eating a very low carb diet on your ability to think clearly.

Now let's see what else the study found.

Unlike many studies of supposedly "low carb" diets, this diet was indeed a very low carb diet with a composition that matched that described in the most recent Atkins book. The nutrient breakdown was:

4% of total energy as carbohydrate, 35% as protein, and 61% as fat (20% saturated fat), with the objective to restrict carbohydrate to less than 20 g/d for the first 8 weeks and with an option to increase to less than 40 g/d for the remainder of the study.

This study also limited saturated fat which is not characteristic of classic Atkins, but the direction the Atkins brand has moved into as it has come to copy South Beach. Over the years the original "Atkins" diet was modified several times to incorporate the techniques found in other bestselling low carb diet books, so this shouldn't be a surprise.

In one major characteristic this diet differ from Atkins as described in the book. From the outset, calories were restricted to "approximately 1433 kcal/d for women and 1672 kcal/d for men."

Those who wish to ignore the findings of the study completely have pointed to this limitation as if it discredited the results. However, I do not believe this is fair. For overweight and slightly obese people, the calorie levels used here correspond very closely to what many people who have successfully lost weight on the Atkins diet report eating on the online diet support forums, for example, Low Carb Friends once the "easy pounds" lost in the first month or so are gone.

Atkins dieters almost always stall after the first 6 weeks and those who do not have a lot of weight to lose often find they do have to cut back on calories to continue on with weight loss.

So much for the "Atkins diet" used in the study. But when we look at the "low fat" diet, we see something even more interesting. The "low fat" diet is described as having "46% of total energy as carbohydrate, 24% as protein, and 30% as total fat (<8% saturated fat), with the objective to restrict saturated fat intake to less than 10 g/d for the study duration and with the inclusion of an approved food exchange (equivalent to the energy content of 20 g of carbohydrate) between weeks 9 and 52."

This is a very moderate low fat diet, very different from diets like Ornish. And more significantly, this is a diet that is actually quite low in carbohydrate. Working out the 46% ratio of carbohydrate against the 1433 calorie daily intake for women, we find that a woman on this diet would be eating only 165 grams of carbohydrate a day, NOT the 300 grams a day which is so often recommended by dietitians.

This is not an overwhelming carbohydrate intake for a person who has functioning beta cells. And everyone in this study DID have functioning beta cells, since the study excluded people with diabetes, and also eliminated people with cardiovascular disease--which would have probably got rid of participant with undiagnosed diabetes.

The study found that both groups of dieters lost the same average amount of weight at the end of the year, on average about 30 lbs. This full text of the mood study does not explain what the groups starting weights were. This data is probably available in an earlier publication about the same study that reported the physiological rather than psychological findings of this study. You can find it HERE. Unfortunately, free full text is not available for that study.

This earlier report on this same study found that the Atkins dieters ended up with a higher HDL and lower Triglycerides than the Low Fat group, but also higher LDL, though the particle size of the LDL was not investigated.

It also reports the LC group also seems to have lost more body fat: LC: –11.3 ± 1.5 kg; LF: –9.4 ± 1.2 kg; P = 0.3, though this may not be statistically significant.

The physiological study report also found that "Blood pressure, fasting glucose, insulin, insulin resistance, and C-reactive protein decreased independently of diet composition." This means that the choice of diet did NOT have any impact on these parameters though they improved similarly on both diets.

It is a very significant finding that the two diets ended up producing the same blood sugar outcomes, though this has to be viewed with the knowledge that this was a study that did not include people with diabetes.

So far I see nothing to make me question that this was a decently conducted study that has something to teach us about the impact of these diets on people who, if they had any blood sugar abnormalities had the mild ones described as "pre-diabetes"--a group that includes many people who have insulin resistance, but also who have normal beta cells and hence who will never progress to full fledged diabetes.

So what should we make of the finding that mood deteriorated more in people on the Atkins diet than on the low fat diet?

The first thing I note, before I look at mood, is that as is the case in so many diet studies, the drop out rate was high--41%, And slightly more people in the Low Carb arm dropped out than in the Low Fat arm.

This is not the first time we've seen this happen. The drop out rate of the Atkins dieters was only exceeded, very slightly, by that of the extreme Ornish dieters in the JAMA diet bakeoff published back in 2005. In that study the Atkins compliance rate was considerably lower than that of the dieters eating the conventional Weight Watchers diet, though compliance on all diets deteriorated.

This latest study did not measure compliance, but my guess is that by the end of the study, it wasn't very good because it never is on any diet and there is evidence suggesting that "carb creep" is a huge problem, long term, even for people who believe they are eating low carb diets.

But that high drop out rate, with the higher Atkins drop out rate suggests that people eating the diet were not universally thrilled and the mood indicators that the study presents seem to me to point to why.

The study used standardized questionnaires, which like all psychological tools are very fuzzy in concept, but since mood itself is a very fuzzy concept, there isn't any better way to measure it.

The study design has going for it that it used several different tools to measure mood, not just a single one. These were "the POMS,which measures 6 separate aspects of mood, including tension-anxiety, depression-dejection, anger-hostility, vigor-activity, fatigue-inertia, and confusion-bewilderment, and provides a global score of mood disturbance (total mood disturbance score [TMDS]) that is determined by subtracting the vigor-activity score from the sum of the 5 negative mood factors; (2) the Beck Depression Inventory (BDI) and (3) the Spielberger State-Trait Anxiety Inventory (SAI)."

What stands out is that the results of all three measurement tools come out with very similar results. At 8 weeks, all the dieters were considerably happier than when they started their diets. And at 8 weeks, the Low carb dieters were MUCH happier than the low fat dieters according to the Depression-Dejection score, probably because the early weight losses on Atkins are much more dramatic and motivating than the losses on the non-ketogenic diet.

By six months things started to change. Both groups were feeling increased Vigor and Activity at six months, probably because that was the time when they had made most of their weight loss and that weight loss made them feel much better about themselves and more prone to physical activity. But by that point, the measurement tools suggest that the mood of the Atkins dieters is beginning to deteriorate compared to that of the people on the low fat diet.

Anyone who has participated in the online Atkins support groups knows that by 6 months most Atkins dieters have either stalled out completely (usually those who are eating very high calorie intakes in the belief that only carbs matter) or they have gone from dramatic weight losses to losing very, very slowly.

You can see exactly how much real dieters lose on a very low carb diet with the analysis of dozens of real people's posted monthly low carb weight loss experiences you'll find HERE.

Slowing weight loss is characteristic of ALL long term diets no matter what the diet composition, but for the Atkins dieter who saw swift weight loss early on in the diet, the slowdown can be devastating, because most Atkins dieters assume that the extreme changes they have to make in what they eat will be rewarded with huge weight losses like those they experience in the first few weeks. When this doesn't happen, the limitations of the diet are much harder to endure.

Experience in the support group environment reinforces the finding that it is at 6 months into the very low carb diet that people run into serious problems with it. The excitement of eating steak, cheese, and avocados has worn off and unless a person is able to cook and willing to put time into hunting up recipes, the food allowed on the diet can become very boring indeed.

And there is another problem, one that is rarely discussed on the Low Carb support boards:. The early high energy level that enthuses people about the very low carb diet may start to fade out. Some people, in fact, experience thyroid slowing (so-called Euthyroid syndrome) characterized by drops in T3.

My guess is that the finding of this study is real, because it mirrors what I've seen in the support groups. After an initial burst of enthusiasm that lasts about 6 months, a large number of low carb dieters disappear. And even those who lose significant amounts of weight tend to disappear shortly after they stall out for a few months or reach goal, only to show up on the support groups a year later with tales of crashing off the diet and regaining all the lost weight.

Because I did the same thing myself, after 3 years on a very low carb diet, I have a very good appreciation of the process that leads from initial enthusiasm, to depression about the need to eat in a way that is so different from what one might want to eat, and the way that dropping energy levels can lead to giving up entirely.

Since I have diabetes and can't process carbs my choice was NOT to say to heck with it and just live with being fat. But people who don't have diabetes can and do.

So I think the mood issue is real and I think that until it is addressed, people will alway have trouble sticking with a low carb diet, long term, no matter what it's impact on their health if it is too extreme.

And it is that factor of extremeness that I think this study sheds some interesting light on.

If we ignore the issue of "fat" which is really a red herring in these two diets, what we see here is that for people WITHOUT diabetes, there may be a much better outcome in terms of mood with a diet that though it restricts carbs a lot compared to the Standard Diet, doesn't restrict them extremely.

In short, for people who do not have diabetes, a diet of 165 g a day is a huge improvement on one of 300 g a day and may be all that is needed. The women eating that 165 grams of carbs a day did lose the same amount of weight and more importantly, their blood sugar profile and blood pressure did not vary from that of the people eating at much lower levels.

For people WITH diabetes this finding is negated by the fact that few of us can tolerate 165 grams of carbohydrate without seeing very poor blood sugars, ones guaranteed to produce complications.

But what I would take from this study is that it supports the strategy I have been promoting for the past 5 years--one that suggests you cut your carbs down ONLY to the level that gives you safe blood sugars, and no lower.

What that level will be varies from person to person and can only be determined using the strategy described HERE.

More importantly, what this study suggests is that if, like me, you find you can only control your blood sugar by eating at extremely low carbohydrate intake levels--for me it was no more than 50 grams a day with no single meal being higher than 12 g--if you start feeling depressed or rundown, it's time to look into finding a medication that will let you raise your carb intake a bit, but still keep hitting your blood sugar targets without making yourself miserable.

For me, the difference between eating at 100 g a day and 50 g a day is that I can do it, year in and year out, happily. (I'm in year 7 of maintaining a 17% loss of body weight.) But I can only eat 100 g a day using fast acting insulin at some meals.

Not EVERYONE gets depressed or exhausted on a long term low carb diet. The people who stay on these diets for years at a time and write the enthusiastic LC blogs are those who feel better on the diet, not worse. There are quite a few people that match that description, especially among those whose blood sugar is hard to control.

But if you run into problems as your low carb diet hits 8 months, or a year, or two, don't fear turning to medication for help. Insulin, metformin, and for some people Byetta, can make a big difference in how easy it is to control your blood sugar and your weight.

Our goal, after all is health but there is little point in purchasing "health" at the cost of your happiness. If after 6 months of eating a very low carb diet your energy level is low and your mood deteriorating, it's time to start tweaking. Talk to your doctor about adding the safe drugs to your regimen.

Too many people treat using medication as if this were a personal failure. It isn't. The safe medications are is just another set of tools to allow you to live a healthy and happy life.

November 8, 2009

Diabetes Month is here and World Diabetes day is coming, and I am not about to get all excited about either.

Diabetes month is an excuse for the merchants who profit from diabetes to tout their wares. Though the drug store flyers may announce that it is "Diabetes month", I note that the prices of the diabetes test strips they are highlighting haven't gone down a penny-and are twice what they were in 1998 when I started buying them. This price increase is far greater than inflation. Are you earning twice what you earned in 1998?

Diabetes month is an opportunity for nutritionists to be quoted in the media telling us how if we cut all the fat out of our diets and ate healthy grains we wouldn't have diabetes.

Diabetes month is when you will read how children cause their Type 2 diabetes by being lazy, though it is far more likely that the huge increase in the Type 2 diabetes in levels in children too young to have caused it via eating patterns has almost certainly been caused by prenatal exposure to environmental toxins like Bisphenol-A which occurs in detectable levels in many canned foods and juices and, more importantly, in baby bottles sold as "Bisphenol-A free." Other common promoters of diabetes in children and adults are commonly used herbicides and arsenic which have contaminated our water supply and the SSRIs, routinely fed pregnant women, which research has proven raise insulin resistance and cause obesity.

World Diabetes Day is even more useless. A bunch of folks in the online diabetes community have been wasting their energy campaigning for a "blue doodle" on Google for World Diabetes Day. My response to this is, "Why?" The doodle doesn't convey a single bit of useful information to a single person. Which is the reason that World Diabetes Day bothers me.

Because the only reason to "raise awareness" of diabetes, is if the awareness we were raising included the simple, easily conveyed information that could HELP people control their diabetes. Which is does not.

Instead of a blue doodle, how about campainging to see the American Diabetes Association explain on its "tight control" web page that lowering carbohydrates will lower blood sugar safely and effectively. The word "Carbohydrate" still does not appear on the ADA's "tight control" page.

Instead of encouraging people to contribute to the large, bloated charities whose track record for doing anything for people with diabetes is abysmal, why not print and distribute as many copies of the "How to Get Your Blood Sugar Under Control flyer" as possible. I have heard from hundreds of people with all kinds of diabetes who tell me that following the instructions on that flyer has dropped their blood sugars from levels producing A1cs as high as 13% to the normal 5% range.

You will find the link to download the flyer in a format using the blood sugar units your country uses at the bottom of THIS PAGE.

I don't want to raise awareness of diabetes. I want to raise awareness of how to CONTROL diabetes.

Until then, all raising awareness about diabetes does is reinforce the tragically flawed beliefs the population has that diabetes is caused by gluttony and sloth and is the punishment people get for overeating.

This is of course not true. If you want ammunition for countering this misinformation you will find it here:

Diabetes is caused by the fatal combination of specific genes and environmental factors which attack people with those genes. These factors attack people with diabetes genes starting out in the womb and continuing on through life. Dramatic increases in the incidence of diabetes have been associated with a host of chemicals that pollute our environment, including common herbicides and plastics, and widely prescribed psychiatric drugs, many of which are now in trace amounts in our drinking water.

And as we all know by now the high fructose corn syrup, which also invaded our food supply a generation ago, greatly increases insulin resistance because it converts to intracellular liver fat.

The huge increase in the incidence of Type 1 diabetes probably is linked to the invasion of our food supply a generation ago by soy protein, because soy contains substances that damage the lining of the gut and allow food proteins, most notably gluten, to enter the blood stream and provoke antibodies including those that attack the pancreas.

By all means, lets spread "awareness" but let that awareness be of the FACTS. Not the garbled, industry friendly message that the corporate sponsors of these diabetes organizations would prefer the public to hear.

The veterans study is one of two studies that found that aggressive blood sugar control did not appear to make any difference in the likelihood of having a heart attack.

But this new analysis of data from the veteran's study found that aggressive lowering of blood sugar did have a dramatic effect on the likelihood of having a heart attack, but only in people who did not already have evidence of severely hardened arteries as measured by CAC heart scans.

In this study, a subset of the subjects in the veteran's study, 301 type 2 patients, had their degree of artery thickening measured by heart scans, i.e. the coronary artery calcium (CAC) computed tomography test. Participants were then followed over the 7.5-year study for development of cardiovascular end points.

After subjecting their data to an oddball statistical manipulations I won't pretend to understand and hence cannot entirely trust, the researchers came up with the finding that there appears to be a Rubicon of sorts with these heart scan scores.

If patients started the study with CAC scores below 100, aggressive lowering of their blood sugar yielded impressive lowering of their rate of cardiovascular "events." But if they started out with CAC scan values above 100 then aggressively lowering their blood sugar did not change the risk of heart attack.

The actual numbers reported were these:

Among those randomized to intensive treatment, for the subgroup with CAC >100, 11 of 62 individuals had events, while only 1 of 52 individuals with CAC ≤100 had an event.

This suggests that there is a point after which you have permanently damaged your cardiovascular system and that past that point, controlling blood sugar alone won't undo the damage. This makes sense because the CAC scan reports on the amount of calcium deposited in your arteries in the form of plaque, and after you've calcified your arteries past a certain point, they are likely to stay that way.

But if that is your situation, all is not lost. Dr. Davis over at the Heart Scan Blog claims that his patients have improved their CAC scores using interventions that include high dose Vitamin D3, lots of fish oil, Niacin, and cutting out wheat from their diets.

Why fish oil may be so helpful was illuminated by a recently reported study where researchers analyzed plaques removed from people having carotid endarterectomy--the operation where they ream out people's carotid arteries to remove plaques that are preventing blood from getting to their brains.

The researchers report:

All of the fats in the plaques were assessed with mass spectrometry... The plaques of asymptomatic patients [i.e. those having no signs that their brain functions was impaired because of clogged arteries] contained more than twice as much DHA as the symptomatic patients, and about one and a half times as much EPA. Significantly less inflammation was also seen in the carotid atherosclerotic plaques from asymptomatic patients.

Getting back to the veterans study. It is worth remembering that the subjects in the veterans study were mostly elderly people whose blood sugar had been way out of control for many years. If you are recently diagnosed, chances are you have not built up insurmountable levels of plaque in your blood vessels. And if that is true, then lowering your blood sugar aggressively may help prevent heart attack.

It is also worth mentioning that even in studies where aggressive lowering of blood sugar did not prevent heart attack, it did lower the incidence of kidney failure. This alone should make it worth pursuing.

And of course, many of us also have found that lowering our blood sugars very aggressively can prevent or reverse neuropathy.

If your doctor was one who warned you against the "dangers" of lowering blood sugar, make sure to tell your doctor about this latest study--and print out the abstract and take it along. Let the doctor know that one of the major studies being cited as arguing against tight control actually showed aggressive blood sugar lowering caused a dramatic drop in heart attacks in people whose CAC scores were modest when they began the blood sugar lowering.

November 1, 2009

Several new studies, two presented at the 2009 IDF World Diabetes Congress and another published in the journal, Diabetes Care, conclude that the Framingham equation used by most doctors to predict your likelihood of developing heart disease even if you have diabetes.

This topic was discussed at the 2009 IDF World Diabetes Congress. You can read very good summaries of two presentations there, one based on ADVANCE data and another on a study done in Greece, in this article:

...the Framingham and UKPDS risk equations overestimated four-year CHD risk by as much as almost 300%. [i.e. it predicted three times as many cases of heart disease as were actually diagnosed.]

The IDF presentation which was based on the study of a Greek population reported, according to the Heartwire article,

... that in a five-year study of over 900 diabetic patients in Greece, the Framingham and UKPDS risk equations predicted about a 10% incidence of CHD, whereas the actual incidence was significantly lower, at 6.8%.

You can read the abstract of the study based on Hoorn data which was just published in Diabetes Care here:

This study compared the Framingham, UKPDS, and a third formula, SCORE, and concluded

The Framingham and UKPDS prediction models overestimated the risk of first CHD event in all glucose tolerance groups. Overall, the prediction models had a low to moderate discriminatory capacity

. Further analysis revealed that the SCORE equation did the best job of predicting heart disease in people with normal glucose tolerance and that the UKPDS did a slightly better job in the group of people diagnosed with elevated blood sugars, though the UKPDS still overestimated risk in this group too.

The findings of these studies conflicts with the finding published n 2007 of the DECODE study which found the Framingham equation underestimated the risk of heart disease in it's population.

What The Risk Formulas Ignore

After using online calculators to assess my own risk using all three formula cited in the above studies, I noticed that several important parameters are completely missing.

1.The Calculators Rely on Heavily on Cholesterol Ratios However, most interestingly, none of these calculators has factored in statin use or looked at whether long term statin use decreases predicted mortality using any of these risk formulas. My guess is that if they did, you would have heard about it from the drug companies pushing statins.

2.The Calculators Ignore C-Reactive Protein (CRP) Given that there seems to be a strong link between the presence of inflammation as measured by CRP and heart attack, this omission is important.

3.The Calculators Ignore BMI or Other Measures of Obesity. One wonders, again, if this is because they were found NOT to correlate to risk in the studies used to define these formula. This is quite possible, since in my own experience heart disease strikes people of all weights.

Calculate--and Overestimate--Your Own Risk

SCORE uses slightly different formulas for different European populations, but not all appear to be available online. You can find an online SCORE calculator based on data from the UK populations Note that this calculator uses fasting glucose to determine whether someone is diabetic and refuses to calculate risk if they are, because of the assumption--disproven by the research cited above, that everyone with diabetes is very high risk. To use this calculator, use the category that corresponds to your fasting glucose.

SearchThis Blog and Bloodsugar101.com

This is the blog for Blood Sugar 101.

Visit the mainBlood Sugar 101 Web Site to learn more about how blood sugar works, what blood sugar levels cause organ damage, what blood sugar levels are safe and how to achieve those safe blood sugar levels.

Stalled on Your Diet?

Recent Comments

I was diagnosed with diabetes in 1998. Since then I've kept my A1cs in the 5.0-6.0% range using the techniques you'll find explained at The main Blood Sugar 101 Web Site, where you'll also find extensive discussion of the peer-reviewed research that backs up the statements you read here.

I've also published two books on related subjects, Blood Sugar 101: What They Don't Tell You About Diabetes, which was an Amazon Diabetes bestseller for 3 years and Diet 101: The Truth About Low Carb Diets.